DESCRIPTION: The functional behavior of polymorphonuclear neutrophils (PMN) in burn injury has been extensively studied, with evidence of upreulation early and downregulation later. The proposal is based on the hypothesis that early burn injury hypersensitizes PMN signaling via burn-related inflammatory mediators, leading to excessive O2- generation and hydroytic enzyme release. Studies are designed to ascertain the involvement of Ca2+ and phosphorylation signaling in these events. Effects of burn-mediated PMN hyperfunction and its blockade on microvascular and parenchymal tissues in intestine will also be examined. A rat scald burn (25%) model will be used, with/without injection of E. coli., studied 1,3,7 and 10 days post burn.